MK deformations at high shear rate on different surfaces coated with matrix proteins and effect of VWF inhibitors. Cord blood MKs suspended in IMDM were perfused on VWF (in the absence or presence of inhibitors), fibrinogen, collagen, or fibronectin at 1800 s−1 for 10 minutes; then IMDM alone was perfused for 10 minutes. Cell numbers were counted in 10 fields at the end of perfusion (20 minutes) and classified according to the 4 stages defined in Figure 1. Intense cell deformation and proplatelet formation occur on VWF. Cell perfusion on VWF in the presence of GPIb-VWF interaction inhibitors, either a blocking antibody to glycocalicin or an anti-VWF MoAb directed against VWF binding site to GPIb, indicated a major inhibition of MK adhesion to VWF and of subsequent steps, thus abolishing proplatelet formation. Abciximab, blocking the interaction of αIIbβ3 with VWF, prevented proplatelet and platelet formation. MK deformations and proplatelet formation on non-VWF surfaces were minimal in shear conditions as shown for fibrinogen, fibronectin, and collagen.
